Proteomic profiling of circulating β-thalassaemia/haemoglobin E extra-cellular vesicles reveals that association with immunoglobulin induces membrane vesiculation
1
Issued Date
2024-01-01
Resource Type
ISSN
00071048
eISSN
13652141
Scopus ID
2-s2.0-85190808538
Pubmed ID
38613149
Journal Title
British Journal of Haematology
Rights Holder(s)
SCOPUS
Bibliographic Citation
British Journal of Haematology (2024)
Suggested Citation
Phongpao K., Pholngam N., Chokchaichamnankit D., Nuamsee K., Praneetponkang R., Ounjai P., Paiboonsukwong K., Siwaponanan P., Pattanapanyasat K., Svasti J., Srisomsap C., Weeraphan C., Chaichompoo P., Svasti S. Proteomic profiling of circulating β-thalassaemia/haemoglobin E extra-cellular vesicles reveals that association with immunoglobulin induces membrane vesiculation. British Journal of Haematology (2024). doi:10.1111/bjh.19454 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/98158
Title
Proteomic profiling of circulating β-thalassaemia/haemoglobin E extra-cellular vesicles reveals that association with immunoglobulin induces membrane vesiculation
Corresponding Author(s)
Other Contributor(s)
Abstract
Splenectomised β-thalassaemia/haemoglobin E (HbE) patients have increased levels of circulating microparticles or medium extra-cellular vesicles (mEVs). The splenectomised mEVs play important roles in thromboembolic complications in patients since they can induce platelet activation and endothelial cell dysfunction. However, a comprehensive understanding of the mechanism of mEV generation in thalassaemia disease has still not been reached. Thalassaemic mEVs are hypothesised to be generated from cellular oxidative stress in red blood cells (RBCs) and platelets. Therefore, a proteomic analysis of mEVs from splenectomised and non-splenectomised β-thalassaemia/HbE patients was performed by liquid chromatography with tandem mass spectrometry. A total of 171 proteins were identified among mEVs. Interestingly, 72 proteins were uniquely found in splenectomised mEVs including immunoglobulin subunits and cytoskeleton proteins. Immunoglobulin G (IgG)-bearing mEVs in splenectomised patients were significantly increased. Furthermore, complement C1q was detected in both mEVs with IgG binding and mEVs without IgG binding. Interestingly, the percentage of mEVs generated from RBCs with IgG binding was approximately 15–20 times higher than the percentage of RBCs binding with IgG. This suggested that the vesiculation of thalassaemia mEVs could be a mechanism of RBCs to eliminate membrane patches harbouring immune complex and may consequently prevent cells from phagocytosis and lysis.